Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P43026 (lipopolysaccharide)
 62,215 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Histamine and putrescine (a precursor of polyamines) are formed by histidine decarboxylase (HDC) and ornithine decarboxylase (ODC), respectively. Within a few hours after injection of a lipopolysaccharide (LPS) into mice, HDC is induced in the liver, spleen, lung and bone marrow, and ODC is induced in the liver, spleen and bone marrow. Since LPS is known to stimulate the production of various cytokines, the abilities of various cytokines to induce HDC and ODC in the tissues of mice were examined. IL-2, IL-6, IL-8, IFN gamma and M-CSF were ineffective. IL-1 alpha, IL-1 beta, TNF alpha and TNF beta induced HDC and ODC, as does LPS. On the other hand, GM-CSF and G-CSF induced HDC and ODC only in the spleen and bone marrow within a few hours after their injection. These results suggest that, in addition to their roles in inflammation or immune responses, HDC and ODC are also involved in an early stage of hematopoiesis.
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PMID:GM-CSF and G-CSF stimulate the synthesis of histamine and putrescine in the hematopoietic organs in vivo. 138 20

1. An injection of D-galactosamine (GalN) into mice together with a lipopolysaccharide (LPS or endotoxin), interleukin-1 (IL-1) or tumour necrosis factor (TNF), sensitized the mice and induced fulminant hepatitis with severe congestion resulting in rapid death. Since LPS and these cytokines induce ornithine decarboxylase (ODC) and histidine decarboxylase (HDC) in the liver and spleen of mice, the effects of GalN on the induction of ODC and HDC in these organs were examined. 2. The induction of ODC by LPS, IL-1 or TNF was suppressed by GalN in the liver, and this suppression preceded the hepatic congestion. There was good agreement between the degree of hepatic congestion and the suppression of ODC induction by various amounts of GalN. The induction of ODC in the spleen was suppressed only at the highest dose of GalN examined. 3. GalN is known to deplete uridine 5'-triphosphate (UTP), resulting in the suppression of RNA and protein synthesis. An injection of uridine, the precursor of UTP, diminished the GalN-induced suppression of ODC induction by LPS and prevented the hepatic congestion and death. 4. LPS-pretreatment before injection of LPS plus GalN prevented the suppression of ODC activity and prevented the hepatic congestion and death. 5. An injection of putrescine, the product of ODC, prolonged survival time and delayed the development of hepatic congestion. However, injection of an ODC inhibitor into the mice given LPS did not produce hepatic congestion. 6. The induction of HDC in the liver by LPS, IL-1 or TNF was not suppressed by GalN and, at high doses, the response to LPS was enhanced. An inhibitor of HDC neither prevented the hepatic congestion nor enhanced the protective effect of putrescine.7. Although GalN in combination with IL-la induced a markedly higher HDC activity than was observed when it was combined with TNFa, and suppressed the induction of ODC, the former combination at the doses used did not produce hepatic congestion or death. However, the sensitization to TNFa by GalN was markedly potentiated by IL-la.8. These results suggest that suppression of the induction of ODC by GalN may be one cause of the sensitization to LPS, IL-1 or TNF, and that the induction of HDC, i.e. histamine formation, may not be involved in this sensitization.9. These results are consistent with the hypothesis that both IL-1 and TNF are involved in the sensitization to LPS.
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PMID:Ornithine and histidine decarboxylase activities in mice sensitized to endotoxin, interleukin-1 or tumour necrosis factor by D-galactosamine. 147 81

The response of mouse peritoneal macrophages to Escherichia coli lipopolysaccharide (LPS) resulted in induction of histidine decarboxylase (HDC) and, consequently, of histamine production. Concanavalin A had no effect on the reactions. Alpha-fluoromethylhistidine, a suicide inhibitor of HDC, attenuated, in a dose-dependent manner, both spontaneous and LPS-stimulated IL-1 synthesis by macrophages. IL-1 production was significantly blocked by either an H1 anti-histamine, diphenhydramine, or H2 anti-histamine ranitidine, in the absence of any exogenous histamine. Addition of exogenous histamine accentuated the IL-1 production by macrophages as a function of its dose. These results suggest that IL-1 production by mouse peritoneal macrophages is regulated by histamine synthesized in the system per se and that the effect of histamine is dependent on both H1 and H2 histamine receptors located on the surface of the cells.
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PMID:Regulation of interleukin-1 synthesis by histamine produced by mouse peritoneal macrophages per se. 231 55

When spleen cells of C57BL/6 mice or mast cell-deficient W/Wv mice were cultured, their histidine decarboxylase (HDC) activity increased with increases in the histamine concentration in the cells and the medium. Addition of concanavalin A (Con A) or Escherichia coli lipopolysaccharide (LPS) enhanced the increase. The removal of adherent cells reduced both the control HDC activity and the response to the mitogens. Purified T lymphocytes responded to Con A but not to LPS. Neither Con A nor LPS had any effect on B lymphocytes. Treatment of T cells with anti-Thy-1.2 and complement completely abrogated the induction of HDC. Histamine synthesis dependent on Con A by T cells was stimulated by the addition of conditioned medium from peritoneal adherent cells activated with LPS. The addition of recombinant interleukin-1 (rIL-1) or peritoneal adherent cells fixed with paraformaldehyde significantly enhanced HDC induction dependent on Con A in T cells. These results suggest that histamine is synthesized by T lymphocytes through HDC and that the reaction was enhanced by a soluble factor(s) released from macrophages.
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PMID:Histamine synthesis by mouse T lymphocytes through induced histidine decarboxylase. 278 10

The injection of recombinant interleukin-1 (IL-1) into mice induced histidine decarboxylase (HDC) activity in the bone marrow, spleen, lung and liver and ornithine decarboxylase (ODC) activity in the spleen and liver. The ability of IL-1 to induce these responses was the most potent of the various cytokines tested. The induction of these responses by IL-1 seemed to be more rapid than that produced by a lipopolysaccharide. The potency of IL-1 alpha to induce both HDC and ODC activities was similar to that of IL-1 beta, and their combination did not potentiate the induction of these responses. In contrast, although the ability of recombinant tumor necrosis factor-alpha (TNF alpha) to induce these responses was less potent than that of IL-1 alpha or IL-1 beta, the combination of TNF alpha and IL-1 beta produced higher HDC and ODC activities in some tissues tested than those induced by the combination of IL-1 alpha and IL-1 beta. These results suggest that the syntheses of histamine and putrescine are regulated by IL-1 and/or TNF alpha in inflammatory or immune responses. Through these experiments, it was noticed that, in spite of a marked induction of HDC activity in the bone marrow, there was no detectable induction of ODC activity in this tissue. The meaning of HDC induction in the bone marrow is discussed.
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PMID:Induction of histidine and ornithine decarboxylase activities in mouse tissues by recombinant interleukin-1 and tumor necrosis factor. 278 63

When cells of mouse myelomonocytic leukemia cell line, WEHI-3B, were cultured in the presence of actinomycin D plus the serum which was obtained from mice injected with bacterial endotoxin, i.e., lipopolysaccharide, their histidine decarboxylase (L-histidine carboxy-lyase, EC 4.1.1.22) (HDC) activity increased about 100-fold with a peak at 48 h. According to the increase in HDC activity, the expression of surface antigens associated with macrophages, such as Mac II, Mac III and Iad, increased markedly on WEHI-3B cells as well as their morphological changes to macrophages. Histamine levels in the culture medium increased concomitantly with the increase in the HDC activity in WEHI-3B cells, whereas the histamine contents inside the cells did not increase remarkably. Furthermore, the addition of lipopolysaccharide to the culture medium caused an additional 2-fold increase in the HDC activity of WEHI-3B cells. These results indicate that the increase in HDC activity in WEHI-3B cells may represent an event in the process of the differentiation to macrophages.
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PMID:Increase of histidine decarboxylase activity in murine myelomonocytic leukemia cells (WEHI-3B) in parallel to their differentiation into macrophages. 305 14

When spleen cells of C57BL/6 mice were cultured, their histidine decarboxylase (HDC) activity increased with a concomitant increase in the histamine concentration in the culture medium. The addition of concanavalin A (Con A) or E. coli lipopolysaccharide (LPS) to the culture enhanced the responses. Treatment with dexamethasone or corticosterone significantly inhibited both spontaneous and Con A-dependent induction of HDC and histamine biosynthesis. Progesterone and estradiol did not inhibit but rather enhanced the responses. Testosterone had little effect on HDC activity and the histamine level of the culture medium of spleen cells. Adherent cells obtained from glycogen-stimulated peritoneal exudates had the enzyme constitutively. Con A had no appreciable effect on the HDC activity and the histamine level of the culture of these adherent cells. However, the addition of conditioned medium of T + B lymphocytes that had been incubated in the presence of Con A rendered the adherent cells responsive to Con A, leading to an increase in the HDC activity and the histamine level of the culture of the cells. Treatment with dexamethasone largely abrogated the responses. The results suggest that HDC-dependent histamine biosynthesis by peritoneal adherent cells is inhibited by glucocorticoids, which act on the adherent cells per se.
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PMID:Inhibition by glucocorticoids of mitogen-dependent histamine biosynthesis caused by histidine decarboxylase in cultured mouse spleen cells and peritoneal adherent cells. 320 36

Culture of spleen cells of C57BL/6 mice led to a spontaneous increase in activity of histidine decarboxylase (HDC) in the cell and the medium. Concomitantly histamine increased in the cells and, especially, in the medium. Addition of concanavalin A (Con A) or lipopolysaccharide (LPS) to the culture enhanced these processes. There was also a significant Con A-dependent increase in HDC activity and histamine biosynthesis in the culture of spleen cells of genetically mast-cell deficient W/Wv mice. Peritoneal macrophages of C57BL/6J mice had constitutively 11-19-fold as much HDC as T and B lymphocytes when compared on the basis of same number of cells. Con A had no effect on HDC activity when the macrophages were cultured alone. However, co-culture with T lymphocytes, separated from macrophages by a millipore filter membrane (pore size, 0.45 micron), rendered the macrophages responsive to Con A, leading to a notable increase in HDC activity in the cell. Addition of LPS caused a small but significant increase in HDC activity in macrophages, even when the cells were cultured alone. Co-culture with T or B cells enhanced the LPS-dependent increase in HDC activity in macrophages. In contrast, the HDC activity in T and B lymphocytes did not change essentially in the presence of any of these mitogens, even when they were co-cultured with macrophages. These results suggest that histamine is synthesized by non-mast cells through HDC.
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PMID:Histamine synthesis by non-mast cells through mitogen-dependent induction of histidine decarboxylase. 326 12

Injection of mice or rats with lipopolysaccharide (LPS) is associated with an increased secretion of glucocorticoids. The high level of mortality following injection of LPS that is noted in adrenalectomized rats can be reversed by dexamethasone or corticosterone. That histamine may be an endogenous mediator of the release of corticosterone caused by LPS is suggested by an attenuation of this corticosterone response by promethazine, an H1 antihistamine. Additional support that LPS-dependent glucocorticoid secretion is mediated, in part, by histamine, is suggested by spleen cell transfer studies revealing differences in the induction of histidine decarboxylase (HDC) synthesis and corticosterone release by the C3H/HeN and C3H/HeJ strains of mice that are differentially sensitive to LPS effects. These and other data on increased levels of histamine and HDC during mitogen-induced lymphocyte blastogenesis, as well as experiments revealing immunomodulatory effects of histamine and histamine agonists and antagonists on lymphocyte blastogenesis, are consistent with the hypothesis that following infection with gram-negative bacteria, the histamine-induced increase in glucocorticoid secretion results in inhibition of HDC in splenocytes, a concomitant attenuation of histamine production, and a resulting return to immune homeostasis.
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PMID:Significance of increased secretion of glucocorticoids in mice and rats injected with bacterial endotoxin. 333 Jun 74

Escherichia coli lipopolysaccharide (LPS) induced strong time- and dose-dependent secretion of corticosterone (CS) in C3H/HeN mice. In contrast, C3H/HeJ mice were very insensitive to LPS; 100,000 times more LPS was required with C3H/HeJ mice for producing a similar degree of CS secretion as that of C3H/HeN mice. However, C3H/HeJ mice could efficiently respond to other types of stressors, immobilization stress or injection of histamine, a possible mediator of LPS-induced CS secretion (28), leading to a striking increase in the serum levels of CS. Adoptive transfer of spleen cells from C3H/HeN mice converted x-irradiated C3H/HeJ mice to the donor phenotype. Injection of LPS produced a large increase in the activity of histidine decarboxylase (EC 4.1.1.22) in the spleen, lung, and liver of C3H/HeN mice, whereas C3H/HeJ mice were far less responsive. Transfer of spleen cells from the C3H/HeN mice made C3H/HeJ mice sensitive to LPS, leading to an increase in histidine decarboxylase activity in the spleen. There was a statistically significant relationship between the activity of splenic histidine decarboxylase and the serum levels of CS. These results suggest that the LPS-induced secretion of CS is mediated by histamine through induction of histidine decarboxylase in the spleen, lung, and liver. This may be significant in relation to the host-defense mechanism against endotoxemia.
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PMID:LPS-caused secretion of corticosterone is mediated by histamine through histidine decarboxylase. 351 11


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